See also: venous thrombosis - Coumadin
The term thrombus [from thrombos = lump] indicates the presence of a blood clot that adheres to the undamaged walls of the vessels, be they arterial, venous, capillary or coronary (which provide blood supply to the heart).
The presence of a thrombus is a potentially serious condition, as if it reaches a significant size it can obstruct the lumen of the vessel and block its flow.
If the thrombus affects a vein (venous thrombosis - red thrombus) it leads to a circulatory stasis with the appearance of edema, ie an accumulation of fluid in the tissue spaces present between one cell and another, causing an abnormal swelling of the organs or regions concerned . Examples are thrombophlebitis, or superficial thrombosis, and deep vein thrombosis. The first condition manifests itself through the five cardinal signs typical of inflammation (low-grade fever, redness, edema, pain and loss of function), with the characteristic formation of a painful cord along the course of the blocked vein; it rarely gives rise to serious complications due to the formation of emboli. Deep vein thrombosis, on the other hand, is more dangerous, above all because, despite being asymptomatic in about 50% of cases, the thrombus can detach, migrate to the right heart and from there to the lungs.
Often there is a tendency to confuse the meaning of the terms thrombus and embolus or to use them improperly as synonyms. In reality, embolization is a serious complication of thrombosis. In fact, any fragment of thrombus detached from the main thrombotic mass that travels in the bloodstream takes the name of embolus, even if, unfortunately, unfortunately , reaches a smaller diameter vessel occluding it and causing ischemia (ie decrease or suppression of blood flow in a certain area of the body). If the embolus detaches from a venous thrombus it can reach the lungs and obstruct a pulmonary artery (which carries , precisely, venous blood). Both conditions (arterial and venous embolism), are potentially lethal and manifest themselves, respectively, with suffering of the tissues affected by ischemia, up to the compromise of the organs involved (for example, heart attack or stroke), and with chest pain, tachycardia, dyspnea and sudden death.
When the thrombus detaches from a thrombus that has been invaded by pathogenic microorganisms (thromboarteritis suppurativa) it can spread the infection at a distance, causing rapid degeneration and necrosis of the elements of the vessel wall, up to perforating them.
What are the causes of thrombosis?
Blood clotting is a vitally important process that must absolutely remain in balance; if it were not very effective it would in fact cause excessive bleeding, while an increase in haemostatic activity would lead to the formation of thrombus.
The coagulation process is actually given by an "innumerable cascade of chemical reactions in which, in addition to the" famous "platelets and vitamin K, many enzymes and chemical factors participate. This means that at the basis of thrombosis there may be many triggers Among these the most important are represented by the so-called Virchow's triad:
- ENDOTHELIAL DAMAGE,
- STASIS OR TURBULENCE OF THE BLOOD FLOW
- HYPERCOAGULABILITY "OF THE BLOOD.
In arterial and cardiac thrombosis the damaging (endothelial damage due to atherosclerosis) and turbulent factor prevails, while venous thrombi are formed preferably in the presence of blood stasis.
More specifically, venous thrombosis is usually the consequence of one or more of the following risk factors: trauma, surgery, prolonged immobility, varicose veins, infections, lesions of the venous walls, hypercoagulability and venous stasis, infectious diseases, burns, tumors malignancy, old age, estrogen therapy, obesity, pregnancy and childbirth.
Arterial thrombosis generally affects diseased arteries in correspondence with a secondary lesion to atherosclerosis (disease given by the presence of atheromas - obstructive formations conceptually similar to thrombus, but formed by different elements such as cholesterol, macrophages, lipids and calcium crystals -). When the surface wall of the atherosclerotic plaque breaks, a clot forms, just like when we get a wound. Inside the artery the mechanisms of coagulation thus give rise to a hard substance (thrombus or clot) which can interrupt the blood flow causing a sudden enlargement of the plaque. Due to the injury, a small piece of atheroma could also detach which, transported to the periphery by the blood, would occlude smaller vessels (embolism). The main risk factors for the development of arterial thrombosis are therefore of genetic origin (familiarity with the disease) and individual (age, sex, sedentary lifestyle and obesity, smoking, diet rich in cholesterol and saturated fats, stress, poor eating habits and diabetes). Hyperlipidemia, hyperhomocysteinemia and the finding of high levels of antiphospholipid antibodies are associated with an increased risk of thrombosis.
Blood test: antithrombin - prothrombin time INR - thromboplastin time - activated protein C
Antithrombotic treatment and therapy
To be in balance, the coagulation process makes use, as mentioned, of numerous factors. Some of these favor platelet aggregation and the production of fibrin, others, which intervene when the damaged vessel has been repaired, inhibit the aforementioned processes by dissolving the clot.
For the treatment and above all for the prevention of thrombosis, numerous drugs with anticoagulant action are now available which, although acting with different mechanisms of action, have the purpose of "diluting the blood" and limiting platelet aggregation.
